Depression rates skyrocket in adolescence, and adolescent-onset depression is associated with increased risk for depression, substance use, suicide, and work-related disability in adulthood. Consistent with NIH objectives of identifying the biobehavioral causes and prospective trajectories of mental disorders, it is imperative that we identify mechanisms that increase individuals' risk for depression. The long-term goal of this study is to identify the pathways linking early risk factors with adolescent-onset depression; this research will provide a foundation for identification of at-risk youth and the development of interventions to prevent the onset or progression of depression. Specifically, the current study will identify pathways linking high trait negative affectivity (NA) in early adolescence with intermediate biological and cognitive risk factors to predict the rise in depressive disorders in adolescence. We hypothesize that high NA in early adolescence will predict abnormalities in several domains that may constitute intermediate pathways mediating the effects of NA on adolescent-onset depression, particularly (1) abnormal physiological reactivity to stress, particularly poor vagal control and (2) abnormal cognitive processing of stress-related stimuli, particularly selective attention toward negative stimuli; difficulty disengaging attention from stress-related information (e.g. rumination); and negative appraisals of stressful events. We further hypothesize that these abnormalities will prospectively predict depressive symptoms and disorders in adolescence. Both a prospective and a cross-sectional strategy will be used with assessments at screening, baseline, 6-months and 12-months. Youth and parent will complete measures of trait NA and depressive symptoms at screening to determine study eligibility. Youth who are nondepressed at screening with either high-NA (high-risk group) or low-NA (low- risk group) will be invited to participate in the Time 1 laboratory induced stress paradigm before, during, and after which physiological reactivity, state NA, and state cognitive processing will be assessed. Youth and parents will report on depressive symptoms and diagnoses at baseline, 6-months, and 12-months. This prospective design will allow us to test if the effect of trait NA on adolescent-onset depression is mediated by, physiological stress reactivity and/or cognitive processing biases.